Richard G. Hunter, University of Massachusetts Boston
Abstract: Stress is a general term for a unpredictable range of potential threats to an organism's homeostasis. How organisms are able to adapt to a wide variety of unknown stressors with a fixed genome is a fundamental biological challenge. Epigenetic mechanisms have been proposed as an explanation for trait adaptability in response to stress and a substantial literature now supports this idea. Our lab has shown that stress dynamically modulates histone methylation levels in the rat hippocampus and that this modulation has as a principal target, not protein coding genes, but transposons. Transposons are mobile genetic elements, which comprise an order of magnitude larger fraction of the genome than protein coding genes. They represent the largest part of what has been referred to as the "Deep Genome", which has been largely unexplored until recently. We have shown that the expression of a number of transposons are directly regulated by the glucocorticoid receptor. We have also uncovered evidence that some transposon derived RNAs may act upon the glucocorticoid receptor itself, adding complexity to the interactions between corticosteroids, epigenetic mechanisms and the non-coding genome. The rapid regulation of transposon expression by stress suggests a functional role for these elements in stress adaptation in the nervous system, and a role for the deeper genome in the adaptability of organisms to their environment.
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